Description

Product Description

APL180 (also known as L-4F) is a synthetic apolipoprotein A-I mimetic peptide developed to emulate the structural and functional features of natural high-density lipoprotein (HDL) particles. This peptide plays a pivotal role in the modulation of lipid transport, cholesterol efflux, and vascular inflammation. Unlike natural ApoA-I, APL180 offers superior chemical stability and resistance to enzymatic degradation, making it an ideal candidate for biomedical and preclinical studies focused on cardiovascular and metabolic disorders.

The biological relevance of APL180 lies in its ability to replicate the atheroprotective actions of ApoA-I, the main protein constituent of HDL. By binding to lipid molecules and promoting cholesterol efflux from macrophages, APL180 supports reverse cholesterol transport — a crucial process in maintaining lipid balance and preventing arterial plaque accumulation. Moreover, APL180 modulates inflammatory pathways by suppressing cytokine release and reducing oxidative stress markers within endothelial cells.

In addition to its effects on lipid metabolism, APL180 exerts antioxidant and anti-inflammatory effects through the inhibition of lipid peroxidation and the neutralization of reactive oxygen species (ROS). These combined actions make it a valuable research tool for understanding the interplay between lipid regulation, vascular function, and inflammation.

Studies have also demonstrated APL180’s influence on endothelial nitric oxide synthase (eNOS) activity, improving endothelial-dependent vasodilation and vascular homeostasis. Furthermore, the peptide has shown promise in models of atherosclerosis, hyperlipidemia, and metabolic syndrome, where it mitigates plaque formation, improves HDL function, and enhances antioxidant defense mechanisms.

Overall, APL180 provides researchers with a reliable, chemically defined model of ApoA-I function, suitable for exploring new therapeutic strategies in cardiovascular diseases, inflammation, and lipid metabolism.

Product Specifications

Mechanism of Action

APL180 exerts its biological functions through molecular mimicry of apolipoprotein A-I (ApoA-I), a critical component of HDL responsible for reverse cholesterol transport and vascular protection. The amphipathic helical structure of APL180 allows it to associate with lipids and phospholipids, forming HDL-like complexes that facilitate cholesterol efflux from macrophages via the ATP-binding cassette transporters ABCA1 and ABCG1.

This cholesterol efflux is a key mechanism in reducing lipid accumulation within arterial walls and preventing the formation of foam cells — one of the earliest events in atherosclerotic plaque development. In addition, APL180 stimulates lecithin-cholesterol acyltransferase (LCAT) activity, enhancing the maturation of HDL particles and promoting efficient lipid transport.

At the vascular level, APL180 suppresses the expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 while upregulating anti-inflammatory mediators like IL-10. It also reduces the expression of adhesion molecules (VCAM-1, ICAM-1) on endothelial cells, limiting monocyte adhesion and vascular inflammation.

Another important mechanism involves oxidative stress modulation. APL180 scavenges reactive oxygen and nitrogen species, inhibits lipid oxidation, and restores endothelial nitric oxide synthase (eNOS) activity. By improving nitric oxide (NO) bioavailability, it promotes vasodilation and maintains vascular homeostasis.

Recent studies have shown that APL180 influences macrophage polarization, promoting an anti-inflammatory M2 phenotype, which contributes to plaque stabilization. Collectively, these mechanisms make APL180 a potent model compound for studying cardiovascular protection, anti-inflammatory signaling, and HDL functionality.

Side Effects

As a research peptide, APL180 has demonstrated excellent tolerability in preclinical studies. No cytotoxicity or immunogenicity has been reported at standard experimental concentrations. However, in vitro and in vivo data indicate that excessively high doses could potentially lead to cellular lipid depletion or altered membrane fluidity due to enhanced cholesterol efflux.

In experimental animals, transient hypotension or mild vascular relaxation may occur due to increased nitric oxide release. Additionally, metabolic alterations in lipid pathways can occasionally be observed, particularly under prolonged exposure or high-concentration assays.

Researchers are advised to use appropriate dosing and experimental controls to ensure accurate interpretation of results. All applications should be strictly limited to non-clinical, laboratory-based studies.

Disclaimer

All products provided are intended for laboratory research use only and are not for human or veterinary use. No claims are made regarding therapeutic or diagnostic applications. Proper laboratory safety and handling procedures should always be followed.

Keywords

APL180, L-4F, Apolipoprotein A-I Mimetic Peptide, HDL Function, Cholesterol Efflux, Atherosclerosis, Cardiovascular Research, Anti-inflammatory Peptide, Lipid Metabolism, Reverse Cholesterol Transport

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Our trade system provides secure payment processing, verified supplier status, and transparent logistics. Certificates of Analysis (CoA) and HPLC/MS data are available upon request for all peptide batches.